摘要
目的 :研究尼索地平对肾性高血压大鼠 (RHR)左室心肌重构的影响 .方法 :建立RHR模型 ,尼索地平 (1 0mg/kg)灌胃 ,q1 2h ,30d .比较各组间的心质量指数 .取左室壁中段组织 ,常规石蜡切片和超薄切片 ,分别观察心肌显微结构和超微结构的改变 ;天狼猩红染色 ,观察心肌胶原含量和Ⅰ型 /Ⅲ型胶原比值的改变 .结果 :尼索地平仅轻微降低心质量 /体质量和左心室质量 /体质量 (降幅分别为 5 .4 %和 7.7% ,P >0 .0 5 ) ;阻止心肌坏死和炎性浸润 ,减轻心肌细胞肥大 ;电镜下线粒体增生和肿胀的程度明显减轻 ,Z线部分断裂 ,未见明显的间质纤维化 .尼索地平能显著降低胶原容积分数和平均积分光密度 (降幅分别为 6 3.0 %和 6 2 .8% ,P <0 .0 5 ) ,阻止Ⅰ型 /Ⅲ型胶原比值倒置 .结论 :尼索地平对RHR左室重构有一定的保护作用 ,能显著降低胶原增生 ,可同时发挥降血压和改善心脏结构的作用 .
AIM: To study the effects of nisoldipine on the myocardial remodeling of left ventricle in renal hypertensive rats (RHR). METHODS: RHR model was established with nisoldipine (10 mg/kg) ig. 12 h for 30 d and the index of heart was compared between groups. A piece of tissue from the middle of left ventricle was harvested and the paraffin sections and ultrathin sections were prepared routinely. The changes of microstructural and ultrastructural were observed respectively. Picrosirus red staining was performed and the changes of the collagen contents and type Ⅰ to type Ⅲ ratio were determined. RESULTS: Nisoldipine decreased the ratios of heart mass/body mass and left ventricle mass/body mass slightly (by 5.4 % and 7.7 % respectively, P >0.05), stopped the myocardium from necrosis and inflammatory infiltration, and alleviated myocardial hypertrophy. Under transmission electron microscope, the proliferation and swelling of mitochondria were reduced obviously, the Z lines were partially broken, but the field with notable fibrosis was not found. Nisoldipine significantly reduced the collagen volume fraction and the integrity optical density (by 63.0 % and 62.8 % respectively, P <0.05) and kept the ratios of collagen type Ⅰ to collagen type Ⅲ from inverting. CONCLUSION: Nisoldipine plays a protective role in the left ventricle remodeling of hypertension, especially in attenuating the hyperplasia of collagen. Nisoldipine reduces the blood pressure and improves the myocardial structure simultaneously.
出处
《第四军医大学学报》
北大核心
2004年第6期515-518,共4页
Journal of the Fourth Military Medical University
基金
教育部科学技术研究重点项目 (0 2 1 31 )
